Gene therapy can be used to manufacture insulin directly: an oral medication, consisting of viral vectors containing the insulin sequence, is digested and delivers its genes to the upper intestines. Those intestinal cells will then behave like any viral infected cell, and will reproduce the insulin protein. The virus can be controlled to infect only the cells which respond to the presence of glucose, such that insulin is produced only in the presence of high glucose levels. Due to the limited numbers of vectors delivered, very few intestinal cells would actually be impacted and would die off naturally in a few days. Therefore, by varying the amount of oral medication used, the amount of insulin created by gene therapy can be increased or decreased as needed. As the insulin-producing intestinal cells die off, they are boosted by additional oral medications.[76]
When you have type 1 or type 2 diabetes, you need to be very aware of not only what you eat, but also when and how much you eat. A Certified Diabetes Educator (CDE) at Joslin can work with you to develop a healthy meal plan that fits your lifestyle. Following a meal plan can also help you lose weight and lower your risk of developing complications.
It isn’t just keeping blood sugar levels down through insulin control that helps diabetes, but fixing the actual problem causing the diabetes. Addressing just one aspect of the problem (blood sugar or insulin) ignores all the other factors like poor diet, toxins, stress, gut problems, immune issues etc. Instead, this single focuses approach can contribute to the problem, making insulin resistance worse and eventually leading to insulin dependent diabetes when the pancreas shuts down completely. Many doctors and nutrition experts recommend the typical 6-11 servings of complex carbs from whole grain sources daily, suggesting that the fiber helps mitigate insulin response. As I have shown before, 6-11 servings of carbohydrates a day is bad for anyone, but is gasoline on a fire to anyone with an impaired insulin response.
When this happens for a period of time, the cells start to become resistant to the presence of insulin, causing a vicious cycle. The body then releases even more insulin, trying desperately to get the cells to uptake the toxic glucose. The presence of excess insulin in the bloodstream is also toxic and further damages the receptors on these cells. Eventually, the insulin allows the glucose access to your fat cells to get it out of the bloodstream. In other words- Fat isn’t stored as fat in the body- Sugar (from carbohydrates) is stored as fat!

In obese young people, decreased β-cell function has recently been shown to predict deterioration of glucose tolerance (4,78). Additionally, the rate of decline in glucose tolerance in first-degree relatives of type 2 diabetic individuals is strongly related to the loss of β-cell function, whereas insulin sensitivity changes little (79). This observation mirrors those in populations with a high incidence of type 2 diabetes in which transition from hyperinsulinemic normal glucose tolerance to overt diabetes involves a large, rapid rise in glucose levels as a result of a relatively small further loss of acute β-cell competence (3). The Whitehall II study showed in a large population followed prospectively that people with diabetes exhibit a sudden rise in fasting glucose as β-cell function deteriorates (Fig. 5) (80). Hence, the ability of the pancreas to mount a normal, brisk insulin response to an increasing plasma glucose level is lost in the 2 years before the detection of diabetes, although fasting plasma glucose levels may have been at the upper limit of normal for several years. This was very different from the widely assumed linear rise in fasting plasma glucose level and gradual β-cell decompensation but is consistent with the time course of markers of increased liver fat before the onset of type 2 diabetes observed in other studies (81). Data from the West of Scotland Coronary Prevention Study demonstrated that plasma triacylglycerol and ALT levels were modestly elevated 2 years before the diagnosis of type 2 diabetes and that there was a steady rise in the level of this liver enzyme in the run-up to the time of diagnosis (75).

Many studies show that lifestyle changes, such as losing weight, eating healthy and increasing physical activity, can dramatically reduce the progression of Type 2 diabetes and may control Type 1 diabetes. These lifestyle changes can also help minimize other risk factors such as high blood pressure and blood cholesterol, which can have a negative impact on people with diabetes.

Genetic predisposition to liver problems or certain autoimmune diseases often correlate to higher rates of diabetes. This is likely because proper insulin response is handled by the pancreas and liver, so problems here could affect the body’s normal response. Studies have linked certain autoimmune disease and leaky gut syndrome with higher instances of diabetes also, so this correlation is logical as well.
Like trials with any other supplement or herbal product, the primary question we must answer is “What exactly was studied?”. The cinnamon you have in your kitchen may be a single species of plant or a mix of different cultivars. Ceylon cinnamon (Cinnamommum verum) is more commonly found in the West. Cassia cinnamon (Cinnamomum aromaticum) is the version of cinnamon that’s been studied in trials. The chemical hydroxychalcone has been identified as a potential active ingredient, which is believed to modify the sensitivity of cells to insulin, enhancing their uptake. If that’s the true mechanism of action, then it would work in a manner similar to that of the drugs Avandia, Actos, and metformin (Glucophage). Given the active ingredient (or ingredients) have not yet been definitively isolated, the issue of studying cinnamon is problematic. There’s no way to assess the potency of any batch, which complicates any evaluation. And that may be a reason why the research with cinnamon is inconsistent and largely disappointing.
Low glycemic index foods also may be helpful. The glycemic index is a measure of how quickly a food causes a rise in your blood sugar. Foods with a high glycemic index raise your blood sugar quickly. Low glycemic index foods may help you achieve a more stable blood sugar. Foods with a low glycemic index typically are foods that are higher in fiber.
I’m glad you talk about personal tolerance. My doc wants me to go on a ketogenic diet, but even when on the Autoimmune Paleo Diet, my adrenals would go a bit nuts. I can’t go any longer than 6 hours without food overnight…my adrenals start pumping out the adrenalin after about 3 to 6 hours of sleep (no matter what I eat or don’t eat before bed) and I wake up with anxiety. Adding a bit of carbs (3/4 cup at dinner and 1/2 cup at lunch) has allowed me to go a full 6 hours (would love 7 or 8) but it still feels terrible when I wake up.
In that analysis, the Khan study looks like an outlier. More studies have emerged since then: Crawford in 2009 found 1g of cinnamon per day reduced A1C levels compared to placebo. Suppapitiporn found no effect on any measure with 1.5g per day. Akilen, in 2010, found an effect with 2g per day. Another meta-analysis, published in 2012 and included 6 studies, concluded the opposite of Baker, and made positive conclusions:
1. Avoid toxins as much as possible: There is no doubt that we live in a polluted world, and it is next to impossible to avoid all toxins, however, recent research suggests that environmental toxins such as pesticides in our food and drinking water can be factors in causing or worsening Type 1 Diabetes. To lessen the amount of toxins that enter the body, try to buy “green” cleaners, organic fruits and vegetables, and dairy that is from organic or grass-fed cows. Although these items may be a bit more expensive, the health benefits are well-worth the higher price tag.
By checking your own blood sugar levels, you can track your body's changing needs for insulin and work with your doctor to figure out the best insulin dosage. People with diabetes check their blood sugar up to several times a day with an instrument called a glucometer. The glucometer measures glucose levels in a sample of your blood dabbed on a strip of treated paper. Also, there are now devices, called continuous glucose monitoring systems (CGMS), that can be attached to your body to measure your blood sugars every few minutes for up to a week at a time. But these machines check glucose levels from skin rather than blood, and they are less accurate than a traditional glucometer.
Practitioners agree that nutrition is the cornerstone of diabetes management, and that a range of nutrition intervention strategies can be used to meet the metabolic goals and individual preferences of the person with diabetes. However, there are significant differences in the approach and methodologies used by alternative and conventional practitioners to manage the disease. One difference is in terminology. When is remission really remission?
"Perfect glycemic control" would mean that glucose levels were always normal (70–130 mg/dl, or 3.9–7.2 mmol/L) and indistinguishable from a person without diabetes. In reality, because of the imperfections of treatment measures, even "good glycemic control" describes blood glucose levels that average somewhat higher than normal much of the time. In addition, one survey of type 2 diabetics found that they rated the harm to their quality of life from intensive interventions to control their blood sugar to be just as severe as the harm resulting from intermediate levels of diabetic complications.[17]

The NIDDK has played an important role in developing “artificial pancreas” technology. An artificial pancreas replaces manual blood glucose testing and the use of insulin shots or a pump. A single system monitors blood glucose levels around the clock and provides insulin or a combination of insulin and a second hormone, glucagon, automatically. The system can also be monitored remotely, for example by parents or medical staff.

As of now, diabetes is classified as either Type I or Type II. New research suggests there are several more types of diabetes, which all require different treatment approaches, but that’s a developing area of knowledge. On an episode of Bulletproof Radio, Dr. Steven Masley explains why doctors are starting to view Altzheimer’s disease as “type III diabetes” and picks apart the relationship between insulin and brain degeneration. Listen to it on iTunes.

The earliest predictor of the development of type 2 diabetes is low insulin sensitivity in skeletal muscle, but it is important to recognize that this is not a distinct abnormality but rather part of the wide range expressed in the population. Those people in whom diabetes will develop simply have insulin sensitivity, mainly in the lowest population quartile (29). In prediabetic individuals, raised plasma insulin levels compensate and allow normal plasma glucose control. However, because the process of de novo lipogenesis is stimulated by higher insulin levels (38), the scene is set for hepatic fat accumulation. Excess fat deposition in the liver is present before the onset of classical type 2 diabetes (43,74–76), and in established type 2 diabetes, liver fat is supranormal (20). When ultrasound rather than magnetic resonance imaging is used, only more-severe degrees of steatosis are detected, and the prevalence of fatty liver is underestimated, with estimates of 70% of people with type 2 diabetes as having a fatty liver (76). Nonetheless, the prognostic power of merely the presence of a fatty liver is impressive of predicting the onset of type 2 diabetes. A large study of individuals with normal glucose tolerance at baseline showed a very low 8-year incidence of type 2 diabetes if fatty liver had been excluded at baseline, whereas if present, the hazard ratio for diabetes was 5.5 (range 3.6–8.5) (74). In support of this finding, a temporal progression from weight gain to raised liver enzyme levels and onward to hypertriglyceridemia and then glucose intolerance has been demonstrated (77).
Most of those foods are refined, processed starches and sugars. Lots of diets place people on a restricted plan that doesn’t allow the refined, processed starches and sugars, and people lose weight, regain good BG control and feel better. However, in most cases, the weight comes back and weight creeps up and BG begins rising again due to the inability to sustain many of these diets.
When islet cells have been transplanted via the Edmonton protocol, insulin production (and glycemic control) was restored, but at the expense of continued immunosuppression drugs. Encapsulation of the islet cells in a protective coating has been developed to block the immune response to transplanted cells, which relieves the burden of immunosuppression and benefits the longevity of the transplant.[72]
Grains: Grains, especially gluten-containing grains like wheat, contain large amounts of carbohydrates that are broken down into sugar within only a few minutes of consumption. Gluten can cause intestinal inflammation, which affects hormones like cortisol and leptin, and can lead to spikes in blood sugar. I recommend removing all grains from your diet for 90 days as your body adjusts to this healing program. Then you can try bringing sprouted ancient grains back into your diet in small amounts.

Diet management allows control and awareness of the types of nutrients entering the digestive system, and hence allows indirectly, significant control over changes in blood glucose levels. Blood glucose monitoring allows verification of these, and closer control, especially important since some symptoms of diabetes are not easy for the patient to notice without actual measurement.

The earliest predictor of the development of type 2 diabetes is low insulin sensitivity in skeletal muscle, but it is important to recognize that this is not a distinct abnormality but rather part of the wide range expressed in the population. Those people in whom diabetes will develop simply have insulin sensitivity, mainly in the lowest population quartile (29). In prediabetic individuals, raised plasma insulin levels compensate and allow normal plasma glucose control. However, because the process of de novo lipogenesis is stimulated by higher insulin levels (38), the scene is set for hepatic fat accumulation. Excess fat deposition in the liver is present before the onset of classical type 2 diabetes (43,74–76), and in established type 2 diabetes, liver fat is supranormal (20). When ultrasound rather than magnetic resonance imaging is used, only more-severe degrees of steatosis are detected, and the prevalence of fatty liver is underestimated, with estimates of 70% of people with type 2 diabetes as having a fatty liver (76). Nonetheless, the prognostic power of merely the presence of a fatty liver is impressive of predicting the onset of type 2 diabetes. A large study of individuals with normal glucose tolerance at baseline showed a very low 8-year incidence of type 2 diabetes if fatty liver had been excluded at baseline, whereas if present, the hazard ratio for diabetes was 5.5 (range 3.6–8.5) (74). In support of this finding, a temporal progression from weight gain to raised liver enzyme levels and onward to hypertriglyceridemia and then glucose intolerance has been demonstrated (77).

As of 2015 the guidelines called for an HbA1c of around 7% or a fasting glucose of less than 7.2 mmol/L (130 mg/dL); however these goals may be changed after professional clinical consultation, taking into account particular risks of hypoglycemia and life expectancy.[18][19] Despite guidelines recommending that intensive blood sugar control be based on balancing immediate harms and long-term benefits, many people – for example people with a life expectancy of less than nine years – who will not benefit are over-treated and do not experience clinically meaningful benefits.[20]
Like the sulfonylureas, meglitinides is a class of drugs that work by promoting insulin secretion from the pancreas. Unlike the sulfonylureas, which last longer in the body, repaglinide (Prandin) and nateglinide (Starlix) are very short acting, with peak effects within one hour. For this reason, they are given up to three times a day just before meals.